Geraniin inhibits proliferation and induces apoptosis through inhibition of phosphatidylinositol 3-kinase/Akt pathway in human colorectal cancer in vitro and in vivo.

Geraniin, a polyphenolic component isolated from Phyllanthus amarus, has been reported to possess diverse biological activities, including antitumor, antiinflammatory, antihyperglycemic, antihypertensive, and antioxidant. However, the role and underlying mechanisms of geraniin in colorectal cancer still remain unclear. In the present study, we found that geraniin notably inhibited cell proliferation and clonogenic formation of colorectal cancer cell SW480 and HT-29 in a dose-dependent manner by Cell Counting Kit 8, EdU, and colony formation assays, respectively. Additionally, geraniin remarkably induced apoptosis of SW480 and HT-29 cells in a dose-dependent way by Hoechst 33342 staining, flow cytometric analysis, and TdT-mediated dUTP nick-end labeling assays and increased the expressions of Bax, caspase-3, and caspase-9, while decreased the level of Bcl-2. Besides, wound healing, transwell migration, and invasion assays demonstrated that geraniin obviously inhibited the migration and invasion of SW480 and HT-29 cells. Moreover, it also inhibited the levels of phospho (p)-phosphatidylinositol 3-kinase and p-Akt. Furthermore, in-vivo animal study revealed that geraniin had the significant inhibitory effects on tumor growth and promoted cancer cell apoptosis remarkably, which further confirmed the antitumor effect of geraniin. Taken together, the present study exhibited the positive role of geraniin in inhibiting proliferation and inducing apoptosis through suppression of phosphatidylinositol 3-kinase/Akt pathway in colorectal cancer cells in vitro and in vivo, which might provide new insights in searching for new drug candidates of anticolorectal cancer.

Diagnostic value of endoscopic ultrasound elastography for benign and malignant digestive system tumors.

OBJECTIVE: To investigate the effect of endoscopic ultrasound real-time tissue elastography in differential diagnosis of benign and malignant digestive system tumors. METHODS: Forty-two patients with solid tumors of digestive system who were admitted to our hospital between October 2017 and October 2018 were selected. All patients were diagnosed by endoscopic ultrasound real-time tissue elastography. Elastography score was used. The strain ratios (SR) of the lesion and the surrounding control tissues were measured and compared. RESULTS: Lesions with elastography score no more than two points were evaluated as benign, while lesions with elastography score no less than three points were evaluated as malignant. The difference of the elastography score between the benign lesion group and malignant lesion group was statistically significant (P<0.05). The sensitivity, specificity and accuracy of endoscopic ultrasound elastography in the diagnosis of malignant tumors of digestive system were 91.4%, 88.9% and 87.5%, respectively. The SR of the benign lesions ranged from 0.01 to 7.34, with a median SR of 7.33; the SR of the malignant lesions ranged from 1.01 to 47.66, with a median SR of 20.07. The SR of the benign lesions was significantly lower than that of the malignant lesions (P<0.05). CONCLUSION: Elastography of benign and malignant tissues of digestive tract tumors has different image characteristics. Endoscopic ultrasound real-time tissue elastography is effective in differential diagnosis of digestive tract tumors as it can effectively determine whether a tumor is benign or malignant and improve diagnostic accuracy.

Roles of Smad3 and Smad7 in rat pancreatic stellate cells activated by transforming growth factor-beta 1.

BACKGROUND: Pancreatic stellate cells (PSCs) play a major role in promoting pancreatic fibrosis. Transforming growth factor beta 1 (TGF-beta1) is a critical mediator of this process. This study aimed to determine the expression of the Smad3 and Smad7 genes in the process of PSC activation, and explore the mechanisms of chronic pancreatitis. METHODS: The expressions of Smad3 and Smad7 in PSCs before and after TGF-beta1 treatment were detected by reverse transcription-polymerase chain reaction and Western blotting analysis. Smad3 expression was detected in PSCs after treatment with 5 ng/ml of TGF-beta1 for 24 hours. RESULTS: Smad7 expression was decreased in TGF-beta1-activated PSCs (P<0.05) in a dose-dependent manner. When TGF-beta1 concentration reached 10 ng/ml, the expression of p-Smad3, Smad3, and Smad7 was inhibited (P<0.05). CONCLUSIONS: TGF-beta1 promotes the expression of Smad3 and inhibits the expression of Smad7 during the activation of PSCs. In contrast, high-dose TGF-beta1 downregulates the expression of Smad3 in completely activated PSCs.